Topography of cross-sectional and longitudinal glucose metabolic deficits in Alzheimer's disease. Pathophysiologic implications
G. S. Smith, M. J. de Leon, A. E. George, A. Kluger, N. D. Volkow, T. McRae, J. Golomb, S. H. Ferris, B. Reisberg, J. Ciaravino and al. et
Department of Psychiatry, University School of Medicine, NY 10016.
Positron emission tomographic studies of cerebral glucose metabolism have
shown high diagnostic specificity in distinguishing among the degenerative
dementias and differentiating between Alzheimer's disease (AD) and normal
aging. The current investigation was undertaken to characterize the
regional glucose metabolic deficits in AD, using cross-sectional and
longitudinal study designs. All subjects met the National Institute of
Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and
Related Disorders Association criteria for AD (n = 45) or were normal (n =
20), and the AD subjects were subdivided into incipient and mild AD and
moderate plus moderately severe subgroups based on the Global Deterioration
Scale. The subjects underwent a non-contrast computed tomographic scan and
a positron emission tomographic (PETT VI) scan. The AD subjects (n = 14)
and normal control subjects (n = 15) received evaluations 2 to 3 years
after baseline study. The brain regions that show glucose metabolic
deficits cross-sectionally (temporal and parietal association areas, with
lesser degrees of deficit in subcortical gray matter structures), over the
stages of AD, also show further deficits longitudinally within the same AD
subjects. The reduction in glucose metabolism is greater than would be
expected from the degree of brain atrophy. The glucose metabolic deficits
are discussed in the context of neuropathologic findings and
neurotransmitter deficits in AD.
Alzheimer's disease is associated with reduced expression of energy metabolism genes in posterior cingulate neurons
Liang et al.
Proc. Natl. Acad. Sci. USA 2008;105:4441-4446.
ABSTRACT
| FULL TEXT
Positron emission tomography imaging in dementia
HERHOLZ et al.
Br. J. Radiol. 2007;80:S160-S167.
ABSTRACT
| FULL TEXT
Mitoenergetic failure in Alzheimer disease
Parihar and Brewer
Am. J. Physiol. Cell Physiol. 2007;292:C8-C23.
ABSTRACT
| FULL TEXT
Reduced functional brain activity response in cognitively intact apolipoprotein E {varepsilon}4 carriers
Lind et al.
Brain 2006;129:1240-1248.
ABSTRACT
| FULL TEXT
One-Year Change in Cerebral Glucose Metabolism in Patients With Alzheimer's Disease
Hirono et al.
J. Neuropsychiatry Clin. Neurosi. 2004;16:488-492.
ABSTRACT
| FULL TEXT
Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's dementia
Reiman et al.
Proc. Natl. Acad. Sci. USA 2004;101:284-289.
ABSTRACT
| FULL TEXT
Association of Life Activities With Cerebral Blood Flow in Alzheimer Disease: Implications for the Cognitive Reserve Hypothesis
Scarmeas et al.
Arch Neurol 2003;60:359-365.
ABSTRACT
| FULL TEXT
Subcortical Hyperintensities in Alzheimer's Disease: Associated Clinical and Metabolic Findings
Sultzer et al.
J. Neuropsychiatry Clin. Neurosi. 2002;14:262-269.
ABSTRACT
| FULL TEXT
Longitudinal PET Evaluation of Cerebral Metabolic Decline in Dementia: A Potential Outcome Measure in Alzheimer's Disease Treatment Studies
Alexander et al.
Am. J. Psychiatry 2002;159:738-745.
ABSTRACT
| FULL TEXT
Positron Emission Tomography in Evaluation of Dementia: Regional Brain Metabolism and Long-term Outcome
Silverman et al.
JAMA 2001;286:2120-2127.
ABSTRACT
| FULL TEXT
Presenilin-1-associated abnormalities in regional cerebral perfusion
Johnson et al.
Neurology 2001;56:1545-1551.
ABSTRACT
| FULL TEXT
Diffusion and Perfusion MR Imaging in Cases of Alzheimer's Disease: Correlations with Cortical Atrophy and Lesion Load
Bozzao et al.
Am. J. Neuroradiol. 2001;22:1030-1036.
ABSTRACT
| FULL TEXT
Frontal Lobe Hypometabolism Predicts Cognitive Decline in Patients With Lacunar Infarcts
Reed et al.
Arch Neurol 2001;58:493-497.
ABSTRACT
| FULL TEXT
FDG PET Imaging in Patients with Pathologically Verified Dementia
Hoffman et al.
JNM 2000;41:1920-1928.
ABSTRACT
| FULL TEXT
Cortisol Reduces Hippocampal Glucose Metabolism in Normal Elderly, but Not in Alzheimer's Disease
de Leon et al.
J. Clin. Endocrinol. Metab. 1997;82:3251-3259.
ABSTRACT
| FULL TEXT
Preclinical Evidence of Alzheimer's Disease in Persons Homozygous for the {epsilon}4 Allele for Apolipoprotein E
Reiman et al.
NEJM 1996;334:752-758.
ABSTRACT
| FULL TEXT